Test for Leaky Gut and SIBO

The leaky gut and SIBO test is a simple urine test that you take at home, at your own pace, and send to us by mail. The test allows us to determine whether you have leaky gut and/or bacterial overgrowth in the small intestine.

Our reference values are based on urine samples from individuals who tested negative on traditional tests for leaky gut and SIBO. If your test results are above these reference levels, you will receive advice and recommendations based on a holistic perspective, including:

• How to rebalance your gut microbiome
• How to relieve stress on the small intestine
• Lifestyle changes for long-term health

Before sending in your sample, you’ll need to activate your test kit and create an account at mygutfeelinglabs.se. Your results will be delivered to your account within 10 days.

A simple urine sample reveals leaky gut and SIBO – the first step toward greater well-being, with personalized recommendations on diet, supplements, and lifestyle changes.

Leaky Gut: The test begins with you drinking a solution containing lactulose. Normally, only tiny amounts of lactulose pass through the wall of the small intestine. If significant levels of lactulose are detected in the urine, it indicates increased intestinal permeability – also known as leaky gut.

SIBO: Curcumin is a compound that cannot be broken down by the body’s own cells but can only be metabolized by bacteria. If bacteria are present in the small intestine, they will break down the curcumin into hexahydrocurcumin (HHC) and octahydrocurcumin (OHC), which are excreted through the kidneys into the urine during the 90 minute passage through the small gut. These metabolites can then be detected using mass spectrometry.

Leaky gut and SIBO are not classified as diseases or diagnoses, but may underlie a range of health issues.

Based on your test results, you will receive tailored advice and recommendations from a holistic perspective, including:

1. How to rebalance your gut microbiome

2. How to relieve stress on the small intestine

3. Lifestyle changes for long-term health

Take the test today and take the first step toward better well-being and healthy aging.

1. Avoid taking the laxative Lactulose/Duphalac®, Imodium®, Dimor®, Loperamide®, fermented products, curry, turmeric, and curcumin supplements for two days before the test.
2. The test begins with you drinking a solution containing lactulose, glucose, and curcumin. For younger individuals, the dosage may be reduced based on body weight.
3. Collect a urine sample 1.5 hours after drinking the solution.
4. You will receive your results within 2–10 days after your sample reaches our laboratory.

Contents

• Your test kit includes
• Clear instructions on how to perform the test and return the sample.
• Powder containing glucose, curcumin and a solution of lactulose (not lactose).
• Sample tube
• Prepaid return envelope for delivery within Sweden. If you live outside Sweden, please add a stamp.

What does the Leaky Gut and SIBO Test tell me?

We analyze the presence of a well-known marker for leaky gut (lactulose) and bacterial metabolites that accumulate in the bladder during the 90 minutes it takes for the fiber solution to pass through your small intestine. Elevated levels of lactulose indicate increased intestinal permeability (leaky gut), while the presence of specific bacterial metabolites indicates SIBO.

Because our test detects metabolites from a broad range of gut bacteria, we can more reliably determine if bacteria are present in the small intestine. It only takes one metabolite exceeding the reference range for your condition to be classified as SIBO.
If your test result is positive for leaky gut and/or SIBO, you’ll receive personalized dietary and supplement advice, as well as suggestions for lifestyle changes to support your well-being.

What does the Leaky Gut and SIBO Test measure?

The test measures the presence of a well-known marker for leaky gut (lactulose, not to be confused with lactose) and bacterial metabolites that can only be produced by bacteria as the fiber solution passes through the small intestine. The metabolites are detected using a highly advanced mass spectrometry system (Agilent Ultivo).

Why should I test for leaky gut and SIBO?

A sensitive and bloated stomach, food intolerances, joint and muscle pain, eczema, fatigue, brain fog, low mood, headaches, and sugar cravings may all be caused by leaky gut. One common cause of leaky gut is bacterial overgrowth in the small intestine (SIBO), which can develop due to factors such as chronic stress.

Does what I eat in the days before the test affect the results?

Yes, significantly. Avoid taking lactulose-based laxatives (Lactulose/Duphalac®), Imodium®, Dimor®, Loperamide®, fermented foods, curry, turmeric, and curcumin supplements two days before the test.

Can I take probiotic supplements and still do the test?

No. Since our test analyzes bacterial metabolites from bacteria in the small intestine, taking probiotics or synbiotics could affect the results by introducing additional bacteria.

What makes Gutfeeling Labs’ test unique?

We’ve developed a completely new method for detecting leaky gut and SIBO. The test is based on mass spectrometry, identifying both a known marker for leaky gut (lactulose) and bacterial metabolites in a single analysis. This approach is unique on the market, as it measures metabolites from a wide range of bacteria (not just gas-producing ones) and uses a urine sample—allowing metabolites to accumulate in the bladder during the 90 minute passage of the fiber solution’s passage through the small intestine. By this, a significantly higher sensitivity for detecting bacteria in the small intestine is accomplished.

Can children and adolescents take the Leaky Gut and SIBO Test?

Yes—provided there is no allergy or sensitivity to the ingredients. The fiber solution contains compounds found in everyday foods: glucose, curcumin, and lactulose (the latter also forms when milk is heated). The powder is dissolved in a glass of water and the dosage is adjusted according to weight (e.g., adults drink a full glass, someone around 40 kg drinks half a glass, etc.).

Where are the analyses performed?

All analyses are carried out using commercial systems (Agilent) routinely used for clinical testing at the Division of Occupational and Environmental Medicine, Medicon Village, Lund.

Who owns the test results?

The test data belongs to Gutfeeling Labs. We do not sell your test results, data, personal information, or similar. You can read more about how we comply with GDPR in our Privacy Policy.

How soon can I expect results from the recommendations if I test positive for leaky gut and/or SIBO?

This varies greatly—from as little as one day to several months. It depends on how long leaky gut and/or SIBO has been present and how much of the small intestine is affected by SIBO. Our experience is that GutClear® speeds up the recovery.

Can I order a test for someone else?

Yes. The analysis is linked to a specific person and account only when the kit is activated. Instructions for this process are included in the kit.

How fast will I receive my test kit?

Orders are usually shipped the following business day. Delivery via PostNord typically takes 2–3 business days.

How long does the test kit stay valid?

Your test kit can be stored at room temperature for up to 18 months. Once the test is completed, it should be mailed the same day. If that’s not possible, we recommend freezing the sample until it can be sent.

Can this test diagnose diseases?

No, this is not a diagnostic test and cannot be used for medical diagnosis. It identifies conditions in the small intestine, but neither leaky gut nor SIBO are officially recognized medical diagnoses.

Are results affected by pregnancy?

No, pregnancy does not affect the results.

Scientific references organized by research question

Risk factors for the development of SIBO?

Vantrappen, G., Janssens, J., Hellemans, J., & Ghoos, Y. (1977). The interdigestive motor complex of normal subjects and patients with bacterial overgrowth of the small intestine. The Journal of clinical investigation, 59(6), 1158–1166. This study suggests that bacterial overgrowth may be due to a specific motility disorder, i.e., complete or near-complete absence of the migrating motor complex (reduced vagus nerve activity).

Husebye, E., Skar, V., Høverstad, T., Iversen, T., & Melby, K. (1995). Abnormal intestinal motor patterns explain enteric colonization with gram-negative bacilli in late radiation enteropathy. Gastroenterology, 109(4), 1078–1089. Reduced stomach acid appears to be responsible for bacterial colonization in the upper intestine (SIBO) and the worsening of an already established small intestinal bacterial flora. Impaired intestinal motility is most likely an important causal factor in the development of SIBO.

Gabbard, S. L., Lacy, B. E., Levine, G. M., & Crowell, M. D. (2014). The impact of alcohol consumption and cholecystectomy on small intestinal bacterial overgrowth. Digestive diseases and sciences, 59(3), 638–644. Among patients who consumed a moderate amount of alcohol, 58% had a positive lactulose breath test (LBT) compared to 38.9% of people who never drank alcohol. The study showed that even moderate alcohol consumption is a strong risk factor for SIBO.

Jacobs, C., Coss Adame, E., Attaluri, A., Valestin, J., & Rao, S. S. (2013). Dysmotility and proton pump inhibitor use are independent risk factors for small intestinal bacterial and/or fungal overgrowth. Alimentary pharmacology & therapeutics, 37(11), 1103–1111. 

SIBO was mainly due to Streptococcus, Enterococcus, Klebsiella, and E. coli. SIFO was due to Candida. Among those with SIBO, 53% had reduced intestinal motility, and 43% used proton pump inhibitors (PPIs). PPI use (P = 0.0063) and dysmotility (P = 0.0003) were independent significant risk factors (P < 0.05) for SIBO. Symptom profiles were similar between those with and without SIBO/SIFO. Reduced gut motility and use of acid-suppressing PPIs were independent risk factors for SIBO or SIFO and were observed in over 50% of patients with unexplained GI symptoms.

Dukowicz, A. C., Lacy, B. E., & Levine, G. M. (2007). Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterology & hepatology, 3(2), 112–122. SIBO develops when normal homeostatic mechanisms controlling small intestinal bacterial populations are disrupted. The two most common predisposing processes are reduced gastric acid secretion and decreased small bowel motility. Bacterial overgrowth can lead to microscopic mucosal inflammation. Analysis of small bowel biopsies in elderly patients with bacterial overgrowth revealed blunted villi, crypt thinning, and increased intraepithelial lymphocytes. Antibiotic treatment reversed these mucosal changes.

Pros and cons of traditional SIBO testing

Losurdo G, Leandro G, Ierardi E, et al. Breath tests for the non-invasive diagnosis of small intestinal bacterial overgrowth: a systematic review with meta-analysis. J Neurogastroenterol Motil. 2020;26(1):16-28. A meta-analysis showed a sensitivity (true positive rate for SIBO) of only 42% for the lactulose breath test and 54.5% for the glucose breath test.

Lim, J., & Rezaie, A. (2023). Pros and Cons of Breath Testing for Small Intestinal Bacterial Overgrowth and Intestinal Methanogen Overgrowth. Gastroenterology & hepatology, 19(3), 140–146. The SIBO breath test has pros and cons. The authors argue that new methods with higher sensitivity are needed to detect SIBO.

Martins, C. P., Chaves, C. H. A., Castro, M. G. B., Gomes, I. C., & Passos, M. D. C. F. (2017). Prevalence of small intestinal Bacterial overgrowth in patients with gastrointestinal symtoms. Arquivos de gastroenterologia, 54(2), 91–95. Results showed a significant prevalence of bacterial overgrowth in the small intestine using the H₂ test and the H₂/CH₄ breath test (56% and 64%, respectively) in patients with GI symptoms, with higher prevalence in women. Methane alone accounted for positive test results in 18% of patients.

Rezaie, A., Pimentel, M. & Rao, S.S. How to Test and Treat Small Intestinal Bacterial Overgrowth: an Evidence-Based Approach. Curr Gastroenterol Rep 18, 8 (2016). Despite being known for decades, there is still a lack of consensus and clarity on methods to detect SIBO; glucose breath test, lactulose breath test, and small bowel aspiration and culture. However, there is no standardization of these tests and their interpretation.

Lin HC. Small Intestinal Bacterial Overgrowth: A Framework for Understanding Irritable Bowel Syndrome. JAMA. 2004;292(7):852–858. doi:10.1001/jama.292.7.852 As an overarching framework for understanding IBS and other functional disorders, SIBO offers a target for exciting research that could lead to better diagnostic methods and treatment strategies.

Dukowicz, A. C., Lacy, B. E., & Levine, G. M. (2007). Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterology & hepatology, 3(2), 112–122. Recently, interest in SIBO and its potential link to irritable bowel syndrome (IBS) has resurfaced. This comprehensive review discusses the identification and treatment of SIBO.

Can gut bacteria metabolize curcumin?

Tan, S., Rupasinghe, T. W., Tull, D. L., Boughton, B., Oliver, C., McSweeny, C., Gras, S. L., & Augustin, M. A. (2014). Degradation of curcuminoids by in vitro pure culture fermentation. Journal of agricultural and food chemistry, 62(45), 11005–11015. Three metabolites—dihydrocurcumin (DHC), tetrahydrocurcumin (THC), and ferulic acid (FA)—were identified in fermentation cultures of gut bacteria from E. coli strains using mass spectrometry. This study provides important insights into the bacterial metabolism of curcuminoids.

Tan, S., Calani, L., Bresciani, L., Dall'asta, M., Faccini, A., Augustin, M. A., Gras, S. L., & Del Rio, D. (2015). The degradation of curcuminoids in a human faecal fermentation model. International journal of food sciences and nutrition, 66(7), 790–796. This study evaluated curcumin metabolism using an in vitro model with human fecal bacteria. Escherichia strains metabolized curcuminoids into tetrahydrocurcumin (THC) and dihydroferulic acid (DFA). The data provide insights into curcumin's microbial metabolism, indicating bacterial degradation products should be considered in studies of bioavailability and bioactivity.

Luo, M., Han, Y., Chen, Y., Du, H., Chen, B., Gao, Z., Wang, Q., Cao, Y., & Xiao, H. (2024). Unveiling the role of gut microbiota in curcumin metabolism using antibiotic-treated mice. Food chemistry, 460(Pt 2), 140706. Results indicated that gut microbiota can produce active curcumin metabolites. This study improves our understanding of interactions between curcumin and gut microbiota.

Lou, Y., Zheng, J., Hu, H., Lee, J., & Zeng, S. (2015). Application of ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry to identify curcumin metabolites produced by human intestinal bacteria. Journal of chromatography. B, Analytical technologies in the biomedical and life sciences, 985, 38–47. This study describes the metabolic profile of curcumin in the human gut flora. Curcumin undergoes extensive phase I and phase II metabolism. A total of 23 curcumin metabolites were identified in vitro, as well as several novel metabolic pathways in the human gut microbiota system.

Di Meo, F., Margarucci, S., Galderisi, U., Crispi, S., & Peluso, G. (2019). Curcumin, Gut Microbiota, and Neuroprotection. Nutrients, 11(10), 2426. Curcumin undergoes bacterial enzymatic modifications, forming pharmacologically more active metabolites than curcumin itself.

Scazzocchio, B., Minghetti, L., & D'Archivio, M. (2020). Interaction between Gut Microbiota and Curcumin: A New Key of Understanding for the Health Effects of Curcumin. Nutrients, 12(9), 2499. Curcumin reaches the colon and undergoes extensive phase I and II metabolism. First, it is metabolized by phase I enzymes: various reductases introduce reactive and polar groups, yielding active metabolites such as dihydrocurcumin, tetrahydrocurcumin, and hexahydrocurcumin.

Can leaky gut be measured with lactulose?

Cox, M. A., Lewis, K. O., & Cooper, B. T. (1999). Measurement of small intestinal permeability markers, lactulose, and mannitol in serum: results in celiac disease. Digestive diseases and sciences, 44(2), 402–406. Average serum lactulose levels after 1 hour in healthy individuals were significantly lower than in untreated celiac patients. Permeability testing with serum lactulose (compared to mannitol) showed positive results in celiac disease patients.

Gan, J., Nazarian, S., Teare, J., Darzi, A., Ashrafian, H., & Thompson, A. J. (2022). A case for improved assessment of gut permeability: a meta-analysis quantifying the lactulose:mannitol ratio in coeliac and Crohn's disease. BMC gastroenterology, 22(1), 16. Using lactulose for measuring intestinal permeability in screening and monitoring celiac and Crohn’s disease is promising.

Seethaler, B., Basrai, M., Neyrinck, A. M., Nazare, J. A., Walter, J., Delzenne, N. M., & Bischoff, S. C. (2021). Biomarkers for assessment of intestinal permeability in clinical practice. American journal of physiology. Gastrointestinal and liver physiology, 321(1), G11–G17. Using lactulose (in relation to mannitol) is a promising marker for intestinal permeability in adults, and is independent of age, BMI, and gender, according to the authors.

Association between SIBO and IBS?

Takakura, W., & Pimentel, M. (2020). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome - An Update. Frontiers in psychiatry, 11, 664. Due to dysbiosis in the gut microbiome, IBS patients may experience increased gut permeability, impaired motility, chronic inflammation, autoimmunity, reduced bile salt absorption, and altered neural activity in both the enteric and central nervous systems. Consequently, SIBO and IBS share several symptoms such as abdominal pain, bloating, diarrhea, and distension. Dysbiosis may also be linked to neuropsychological symptoms, although more research is needed. This review focuses on the role of the microbiome and SIBO in IBS, and new innovations that may help better characterize bacterial overgrowth.

Ghoshal, U. C., Shukla, R., & Ghoshal, U. (2017). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy. Gut and liver, 11(2), 196–208. these healthy SIBO-positive individuals develop disease later.

Association between SIBO and fibromyalgia

Pimentel, M., Wallace, D., Hallegua, D., Chow, E., Kong, Y., Park, S., & Lin, H. C. (2004). A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing. Annals of the rheumatic diseases, 63(4), 450–452. An abnormal SIBO lactulose breath test is more common in fibromyalgia than in IBS. Unlike IBS, the degree of test abnormality is greater in fibromyalgia and correlates with pain severity.

Is SIBO associated with chronic diseases?

Sroka, N., Rydzewska-Rosołowska, A., Kakareko, K., Rosołowski, M., Głowinska, I., & Hryszko, T. (2022). Show Me What You Have Inside-The Complex Interplay between SIBO and Multiple Medical Conditions-A Systematic Review. Nutrients, 15(1), 90. This review shows multiple studies confirming associations between SIBO and gastrointestinal, cardiovascular, endocrine, neurological, renal, connective tissue, and dermatological disorders. Further research is crucial to verify the many facets of SIBO. Antibiotic treatment may reduce not only GI symptoms but also manifestations in other organ systems, improving quality of life. This could pave the way for new treatment directions for many chronic conditions.

Connections between SIBO and rosacea (facial eczema)

Drago, F., Ciccarese, G., Indemini, E., Savarino, V., & Parodi, A. (2018). Psoriasis and small intestine bacterial overgrowth. International journal of dermatology, 57(1), 112–113. Patients with psoriasis and rosacea may benefit from small bowel antibiotics targeting SIBO.

Weinstock, L. B., & Steinhoff, M. (2013). Rosacea and small intestinal bacterial overgrowth: prevalence and response to rifaximin. Journal of the American Academy of Dermatology, 68(5), 875–876. A total of 32 out of 63 rosacea patients had SIBO, compared with 7 of 30 community controls and 3 of 30 completely healthy controls. Of the 32 SIBO-positive patients, 28 were treated with rifaximin: 46% reported marked improvement, 25% moderate improvement, and 11% slight improvement in rosacea. All four with ocular rosacea reported marked improvement. Rosacea was unchanged in 18%.

Parodi, A., Paolino, S., Greco, A., Drago, F., Mansi, C., Rebora, A., Parodi, A., & Savarino, V. (2008). Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 6(7), 759–764. SIBO prevalence was higher in rosacea patients (52 of 113) compared to controls (3 of 60). After rifaximin treatment, skin lesions disappeared in 20 of 28 patients and improved significantly in 6. The study shows significantly higher SIBO prevalence in rosacea patients. Those who became SIBO-negative had nearly complete resolution of rosacea maintained for at least 9 months.

Drago, F. et al. The role of small intestinal bacterial overgrwoth in rosaca: A 3-year follow up. J. Am Acad Dermatol Sept 2016. Three-year follow-up of patients with rosacea who were treated with the small intestine-targeted antibiotic rifaximin showed that 64% of patients remained in remission (symptom-free). SIBO appears to play a role in the initiation of rosacea, and a 10-day course of rifaximin proved effective in keeping rosacea under control for up to three years.

How do botanical antimicrobial supplements compare to antibiotic drugs in SIBO?

Chedid, V., Dhalla, S., Clarke, J. O., Roland, B. C., Dunbar, K. B., Koh, J., Justino, E., Tomakin, E., & Mullin, G. E. (2014). Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Global advances in health and medicine, 3(3), 16–24. Botanical supplements with antibacterial properties may be as effective as the drug rifaximin for treating SIBO.

Is there a link between leaky gut and autoimmunity?

Paray, B. A., Albeshr, M. F., Jan, A. T., & Rather, I. A. (2020). Leaky Gut and Autoimmunity: An Intricate Balance in Individuals Health and the Diseased State. International journal of molecular sciences, 21(24), 9770. The traditional model of autoimmune development has recently been challenged by the introduction of a third component: intestinal barrier function, opening up innovative and unexplored treatment strategies for these serious diseases.

Christovich, A., & Luo, X. M. (2022). Gut Microbiota, Leaky Gut, and Autoimmune Diseases. Frontiers in immunology, 13, 946248. The gut microbiota may play a key role in the development of autoimmune processes, likely due to its ability to negatively affect the intestinal barrier.

Does intestinal mucus play a role in the development of chronic diseases?

Johansson, M. E., Sjövall, H., & Hansson, G. C. (2013). The gastrointestinal mucus system in health and disease. Nature reviews. Gastroenterology & hepatology, 10(6), 352–361. The mucus system of the gastrointestinal tract is the first line of defense against bacteria, and its organization varies along the gut. In the small intestine, mucus is transported with trapped bacteria toward the colon by intestinal motor activity. In the colon, a two-layered mucus system protects against a significantly higher bacterial load, with the inner layer normally remaining impenetrable to bacteria.

Connections between gut microbiota and chronic diseases

Creely SJ, McTernan PG, Kusminski CM, Fisher M, Da Silva NF, Khanolkar M, Evans M, Harte AL, Kumar S 2007. Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. Am J Physiol Endocrinol Metab 292:E740 –E747. Circulating bacterial toxins (LPS) are elevated in the plasma of patients with type 2 diabetes compared to lean, healthy individuals. LPS activated the innate immune system, releasing pro-inflammatory mediators IL-6 and TNF-alpha. Gut microbiota may contribute to disease development in overweight individuals with type 2 diabetes via immune stimulation from gram-negative bacterial LPS.

Manco, M., Putignani, L., & Bottazzo, G. F. (2010). Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk. Endocrine reviews, 31(6), 817–844. Systemic exposure to LPS from gram-negative bacteria may cause "metabolic endotoxemia," marked by low-grade inflammation, insulin resistance, and increased cardiovascular risk. LPS triggers immune cascades resulting in pro-inflammatory molecules that disrupt glucose and insulin metabolism, promote atherosclerosis, and contribute to fatty liver disease.

Pussinen, P. J., Havulinna, A. S., Lehto, M., Sundvall, J., & Salomaa, V. (2011). Endotoxemia is associated with an increased risk of incident diabetes. Diabetes care, 34(2), 392–397. Findings suggest that microbes may play a role in diabetes development. Subjects with prevalent diabetes (n = 537) and incident diabetes (n = 462) had higher bacterial endotoxin activity than non-diabetic individuals. Diabetes was associated with endotoxemia, indicating a link between metabolic disorders and inflammation.

Connections between gut microbiota and neurological diseases

Murros, K. E., Huynh, V. A., Takala, T. M., & Saris, P. E. J. (2021). Desulfovibrio Bacteria Are Associated With Parkinson's Disease. Frontiers in cellular and infection microbiology, 11, 652617. The gut bacterium Desulfovibrio is linked to mechanisms that may cause toxic accumulation of the “Parkinson's protein” alpha-synuclein.

Zhan, X., Stamova, B., & Sharp, F. R. (2018). Lipopolysaccharide Associates with Amyloid Plaques, Neurons and Oligodendrocytes in Alzheimer's Disease Brain: A Review. Frontiers in aging neuroscience, 10, 42. LPS is associated with the “Alzheimer's protein” amyloid.

Kim, H. S., Kim, S., Shin, S. J., Park, Y. H., Nam, Y., Kim, C. W., Lee, K. W., Kim, S. M., Jung, I. D., Yang, H. D., Park, Y. M., & Moon, M. (2021). Gram-negative bacteria and their lipopolysaccharides in Alzheimer's disease: pathologic roles and therapeutic implications. Translational neurodegeneration, 10(1), 49. The pathological localization of LPS in the CNS of Alzheimer’s patients suggests a unique role for LPS in Alzheimer's disease. LPS is directly involved in pathology including neuroinflammation via microglia and neuronal cell death through TLR4 signaling.

Lukiw W. J. (2016). Bacteroides fragilis Lipopolysaccharide and Inflammatory Signaling in Alzheimer's Disease. Frontiers in microbiology, 7, 1544. LPS from Bacteroides fragilis is associated with Alzheimer’s disease.

Pogue, A. I., Jaber, V. R., Sharfman, N. M., Zhao, Y., & Lukiw, W. J. (2022). Downregulation of Neurofilament Light Chain Expression in Human Neuronal- Glial Cell Co-Cultures by a Microbiome-Derived Lipopolysaccharide-Induced miRNA-30b-5p. Frontiers in neurology, 13, 900048. Toxins (LPS) from bacteria cause weakening of the internal skeleton structure of nerve cells.